pancreatitis presentation

1. Morning Report
Karim Zawdeh PGYII
Internal Medicine Department

2. Case Presentation
• A 48-year-old man presents to the emergency department with
epigastric pain, nausea, non-bloody vomiting, and anorexia.
• He describes the pain as constant, with a sharp, stabbing nature.
Lying in a fetal position alleviates the pain.
• He has no fever, chest pain, dyspnea, or recent weight loss.
• The pain started suddenly 2 days ago while he was at work. It
progressively worsened, and he was unable to keep down oral intake.
He had similar symptoms 2 months earlier; however, they were mild
and resolved spontaneously.

3. Past medical
• Poorly controlled type 2 diabetes,
• Obesity
• Hypertension,
• Hypothyroidism
• Obstructive sleep apnea on CIPAP.
He has not had any surgeries in the past.
He does not smoke cigarettes
He drinks 1-2 glasses of wine on the weekend.
He reports no illicit drug use

4. Medications
• amlodipine (5 mg daily),
• levothyroxine (100 µg daily)
• metformin (500 mg twice daily).
He denies any new medications or changes to his current ones.

5. Physical Examination
The patient is alert and oriented.
He lies sideways in bed in mild distress due to the pain.
Vitals: afebrile, HR 108 , BP 88/59, RR 24 breaths/min, SPO2 98% on
room air.
• Cardiac and Respiratory examinations are normal.
• The abdominal examination is significant for epigastric tenderness
and decreased bowel sounds, but his abdomen is otherwise soft,
without any guarding or rebound tenderness.

6. Labs
Variable Result Range
Hb 15 13-17
Hct 47% 40-54
Wbc 14,2 5-10
Plt 420,000 135000-
337000
BUN 34 7-20
Creatinine 1.5 0.8-1.5
Variable Result Range
Lactic Acid 3.7 4.5-19.8
ALT 54 20-60
AST 43 6-34
ALK ph 96 44-147
Bil T 0.4 0.1-1.2
Lipase 874 8-54

7. CT of the abdomen and
pelvis with (IV) contrast
• shows moderate peripancreatic
edema, consistent with acute
pancreatitis .
• A 3 × 2 × 2.5 cm septated cyst is
present in the tail of the pancreas.
No pancreatic ductal dilatation is
noted. The gallbladder is normal,
without biliary ductal dilation.

8. Additional Labs
Variable Result Range
ANA 1:40 Positive
Igg4 187 8-140
Total cholesterol 278 <200
Triglyceride 921 <150
Ca 9.9 8-10

9. Question
Based on these findings only, which is the most likely diagnosis?
oAutoimmune pancreatitis
oDrug-induced pancreatitis
oTriglyceride-induced pancreatitis
oAlcoholic pancreatitis
oHereditary pancreatitis

10. Autoimmune
pancreatitis
It has two subtypes:
• Type 1, or lymphoplasmacytic sclerosing pancreatitis,
which is the most common type, is characterized
histologically by lymphocyte and plasma cell infiltration
with fibrosis.
• It usually presents in older men with obstructive
jaundice, with or without a pancreatic mass; diffuse
pancreatic enlargement on imaging; and pancreatic
ductal strictures.
• It is associated with elevated serum IgG4 (more than
two times the upper limit of normal) and can present
as an isolated disease or as part of an IgG4-related
systemic disorder with other organ involvement, such
as the biliary system, lacrimal and salivary glands,
kidneys, lymph nodes, and retroperitoneum.

11. Autoimmune Pancreatitis
• The patient in this case is relatively young,
• with a serum IgG4 level less than twice the upper limit of normal,
and
• he has a normal bilirubin level.
• He also has no other organ involvement besides the pancreas and no
family history of inflammatory bowel disease.
• His imaging studies show no evidence of pancreatic masses or diffuse
enlargement.
• Thus, autoimmune pancreatitis is less likely.

12. Drug
Induced
Pancreatitis
Drug-induced pancreatitis is
unlikely because none of his
medications are known to cause
pancreatitis.
In addition, his alcohol intake is
not high enough to cause
alcoholic pancreatitis

13. Triglyceride Induced Pancreatitis
• Accounts for 4% of all episodes of acute pancreatitis and as many as
56% of cases in pregnancy.
• The risk for pancreatitis is 5% at triglyceride levels > 1000 mg/dL and
10%-20% at levels > 2000 mg/dL.
• A triglyceride level > 1000 mg/dL has been used as a cutoff for the
diagnosis; however, the risk for pancreatitis progressively increases
with serum levels and can occur even at levels as low as 400 mg/dL.

14. Etiology
The etiology of elevated triglycerides is divided into primary and
secondary causes.
• Primary causes are genetic mutations in lipid metabolism that
lead to severe hypertriglyceridemia and can predispose to
pancreatitis.
• These include Fredrickson classification type I, IV, and V
dyslipidemias, also known as familial hyperchylomicronemia,
familial hypertriglyceridemia, and combined
hypertriglyceridemia, respectively.
• Secondary causes of elevated triglycerides are environmental
and include poorly controlled diabetes, obesity,
hypothyroidism, and alcohol use disorder.
• Moreover, some medications have been implicated in
hypertriglyceridemia leading to pancreatitis, including
estrogens, clomiphene, tamoxifen, propofol, beta-blockers,
protease inhibitors, olanzapine, mirtazapine, valproic acid, and
isotretinoin.

15. Clinical
presentation
The clinical presentation of triglyceride-induced pancreatitis is
usually similar to that of pancreatitis from other causes, with
epigastric abdominal pain that typically radiates to the back and
is associated with nausea and vomiting.
However, the course of the disease tends to be more
complicated, and the incidence of pancreatic necrosis, abscess
formation, sepsis, and organ failure is higher than in pancreatitis
from other causes.
Physical examination can reveal lipemia retinalis, xanthelasmas,
xanthomas over extensor surfaces of the extremities, and
hepatomegaly from fatty infiltration of the liver.
The serum amylase level can be falsely normal owing to the
interference of triglycerides with the assay, and serial dilutions
are required to correct it

16. Assessment
for
worrisome
features
Worrisome features in patients with HTGP include the following:
Hypocalcemia
Lactic acidosis
Signs of worsening systemic inflammation (two or more):
Temperature >38.5°C or <35.0°C
Heart rate of >90 beats/min
Respiratory rate of >20 breaths/min or partial pressure of carbon
dioxide (PaCO2) of <32 mmHg
White blood cell (WBC) count of >12,000 cells/mL, <4000 cells/mL, or
>10 percent immature (band) forms
Signs of worsening organ dysfunction or multi-organ failure as defined
by Modified Marshall scoring system for organ dysfunction

18. Management
• Management of triglyceride-induced
pancreatitis involves treatment of the acute
pancreatitis and lowering the triglyceride
levels to < 400 mg/dL.
• Medications that can contribute to
hypertriglyceridemia should be discontinued.
• Risk stratification of acute pancreatitis should
be done early on admission to assess the
severity of pancreatitis , Systemic
Inflammatory Response Syndrome (SIRS)
criteria, and/or Modified Marshall Score.

19. Managemenent
• Initial management of pancreatitis includes supportive
measures, with aggressive IV hydration, analgesia, and
bowel rest.
• If the patient has severe pancreatitis and prolonged fasting
is expected, pancreatic rest with nasojejunal enteral
feeding or total parenteral nutrition should be considered.
• Dietary fat restriction , When patients can tolerate
nutrition by mouth, dietary fat should be severely restricted
(<5 percent fat) until triglyceride levels are <1000 mg/dL

21. Plasmapheresis
the use of plasmapheresis is reserved to
patients with HTGP with worrisome features.
• A single session of plasmapheresis has been
reported to lower triglyceride levels by 50 to
80 percent.
• Triglycerides should be measured after each
cycle of plasmapheresis . We continue
plasmapheresis until triglyceride levels are
below <500 mg/dL
• However, studies have not shown improved
outcomes or mortality benefit

22. Insulin
• Insulin activates lipoprotein lipase, leading to
enhanced chylomicron and very-low–density
lipoprotein (VLDL) metabolism and lowering of
serum triglyceride levels, usually by 50%-75% in
2-3 days.
• Insulin has been used in patients with severe
pancreatitis, especially in those with diabetes and
concomitant hyperglycemia, although multiple
reports have shown that it is also effective in
patients who do not have diabetes.
• Frequent blood glucose checks are required, and
dextrose infusion is needed as well to maintain
euglycemia. Insulin should be discontinued when
the serum triglyceride level is < 500 mg/dL.

23. Management
• Once the patient is able to tolerate oral
intake, a fat-restricted diet is recommended.
• In addition, triglyceride-lowering agents
should be started; fibrates are the most
effective.
• A reasonable second choice is high-dose
omega-3 fatty acids. Niacin and statins can
be added to the regimen
• however, the risk for adverse events,
including rhabdomyolysis and myopathy, is
higher with combination therapy, especially
fibrates and statins.

24. Back to our
patient
• The SIRS criteria score was 2 and the
Modified Marshall Score was 2. These
scores indicate severe pancreatitis.
• He was admitted to the ICU, and IV
fluids and analgesics were started.
• Given his hyperglycemia and severe
pancreatitis with evidence of end-organ
damage (hypotension, tachycardia, and
leukocytosis), insulin infusions were
initiated, with monitoring of his serum
glucose. Dextrose infusion was also
started once his glucose level was < 180
mg/dL.
• His serum triglyceride level was
measured daily while he was receiving
insulin

25. Follow-up
• After 48 hours, his triglyceride level
dropped to < 500 mg/dL, and the
insulin was discontinued.
• His symptoms also started to
improve.
• He was transitioned to a clear-liquid
diet, then to a low-fat diet, which
he tolerated well.
• Fenofibrate was started, and the
patient was discharged home in
stable condition, with a short
follow-up

26. Thank you